Field of the Inventions
Methods and devices are disclosed herein for therapeutically treating atrial tissue to lessen the effects of mechanical stress on atrial tissue, where reducing mechanical stress in the portion of atrial tissue reduces formation of at least one arrhythmia substrate. In one example, the devices and methods are suitable for minimally invasive surgery. More particularly, methods and devices described herein permit creating an ablation pattern on an organ while reducing excessive trauma to a patient.
Description of the Related Art
Atrial fibrillation surgery requires creation of an ablation or coagulation lesion in atrial tissue. Typically, a physician creates a lesion using energy (including but not limited to radiofrequency, D.C., microwave, cryo, laser or other thermal modalities) to prevent wavelets or electrical signals/impulses that propagate through the cardiac tissue to sustain atrial fibrillation or produce atrial flutter, atrial tachycardia, or other arrhythmia.
Many conventional approaches in applying energy to the cardiac tissue face difficulties in attempting to create a complete lesion pattern that prevents propagation of the electrical impulse across the lesion pattern. Some factors attributable to these difficulties are tissue contact throughout the length of the electrode(s) is/are not consistent causing variability in the transmission of energy throughout the target length of ablated/coagulated tissue. Moreover, surrounding anatomic features also contributes to the difficulty in creating a complete lesion pattern. As a result, an incomplete lesion or lesion pattern includes one or more gaps of viable or semi-viable tissue that allows propagation of wavelets through tissue and through the lesion pattern.
Another factor in the inability of existing thermal ablation systems to create complete curvilinear, transmural lesions is the presence of convective cooling on the opposite surface of the atrium. This convective cooling produces a heat sink that decreases the maximum temperature at this surface thereby preventing the lesions from consistently extending transmurally through the entire wall of the atrium. This is especially relevant during beating-heart procedures in which the coagulation/ablation probe is placed against the epicardial surface, and blood flowing along the endocardium removes heat thus producing a larger gradient between temperature immediately under the electrodes along the epicardium and that the temperature at the endocardium.
Apart from improving treatment of existing cases of atrial fibrillation, there are not many options relating to preventative measures to address the causation of atrial fibrillation. The mechanisms leading to the development of persistent atrial fibrillation are not well known. In addition, the connection between various ablation procedures and long-term outcomes has not been established, in many cases the effectiveness of endocardial ablation outcomes decline over time and often require multiple repeat ablation procedures. Identifying the progression of atrial remodeling that produces persistent AF, treatments and performing treatments to address the effects of this remodeling can provide treatments that are designed to counteract the underlying causes to not only interrupt current atrial fibrillation substrates but also prevent future atrial fibrillation substrates from developing. Treatments based on such remodeling can also help identify target ablation locations to complement pulmonary vein isolation in patients with structural heart disease, enlarged atria, high Body Mass Index (BMI), and/or longstanding complex forms of AF.
Most research and treatments focus on endocardial pulmonary vein isolation (PVI) approaches and ignore the importance of the attachments between the atria and pericardium (e.g. pericardial reflections). In addition, most treatments avoid ablation along the posterior left atrium due to the proximity of the esophagus. These limitations hinder the ability to target anatomic substrates caused by atrial stretch due to mechanical stresses, especially those emanating from the pericardial reflections along the posterior left atrium. The impact of these mechanical stresses to the development and progression of persistent AF is substantial. Understanding stress-induced remodeling and its role in AF progression defines a treatment that addresses current substrates initiating and/or maintaining AF, and reduces the stresses preventing continued remodeling and new substrate development.
Atrial stretch, the enlargement, progression and/or displacement of the atrial tissue due to underlying medical conditions is believed to cause calcium overload, calcineurin activation, and changes in metalloproteinases (MMPs) and Tissue inhibitors of metalloproteinases (TIMPs). In addition, the ATI receptor appears to be involved. Weerasooriya R, et al. Catheter ablation for atrial fibrillation: are results maintained at 5 years of follow-up?J Am Coll Cardiol. 2011; 57:160-6. Atrial stretch also seems to result in inflammation. In preclinical animal models, atrial stretch inducing increased atrial fibrosis causes regional conduction slowing, which may increase the likelihood to develop AF. It is believed that stretch of the atria is a main contributor to atrial remodeling.
In addition, Mitral Valve regurgitation increases pressure in the left atrium and clipping the left atrial appendage may increase pressure in the left atrium leading to atrial stretch and eventually atrial fibrillation. Moreover, use of left atrial appendage occlusion devices often causes the atrium to expand more rapidly causing more atrial stretch which leads to more atrial fibrillation.
Atrial remodeling comprises atrial structural changes. Such changes have been observed in animal models of AF with or without underlying diseases and include (i) atrial enlargement, (ii) cellular hypertrophy, (iii) dedifferentiation, (iv) fibrosis, (v) apoptosis, and (vi) loss of contractile apparatus (myolysis), and changes in size and shape of the mitochondria, disruption of the sarcoplasmatic reticulum, and homogeneous distribution of nuclear heterochromatin. It is believed that atrial structural remodeling is the main contributor for initiation and persistence of atrial fibrillation.
Electrical remodeling, meaning the ability of the tissue to conduct an electrical signal or current, is caused by changes in ionic properties of cardiomyocytes (shortening refractoriness and slowing conduction velocity) due to high atrial rates. It is believed to be completely reversible if sinus rhythm can be restored. Structural remodeling is characterized by loss of cardiomyocytes, alteration in extracellular matrix, and fibrosis; can cause non-homogeneity in electrical propagation, slower conduction velocity, and electrical uncoupling. Structural remodeling is believed to be much less reversible even when sinus rhythm is restored.
Fibrotic diseases are characterized by replacement of normal tissue with a collagen-rich matrix that can disrupt organ function. Studies show that when persistent collagen production outpaces or overwhelms mechanisms that remove collagen, excess collagen is deposited in the extracellular matrix, leading to tissue fibrosis in the tissue. Left atrium stiffness is believed to be an independent predictor of recurrent AF after ablation procedures. A LA stiffness index <65.3 mmHg observed >90% AF free probability versus <45% when the index is >65.3 mmHg. Studies show that atrial fibrosis increases atrial stiffness and worsens the reservoir function and is reported to be a predictor of AF recurrence after ablation procedures.
There remains a need to address current substrates which give rise to atrial fibrillation. There also remains a need to attempt to prevent the formation of new substrates that form as a result of stress induced modification of atrial tissue from underlying medical conditions, which lead to atrial fibrillation.